| Literature DB >> 27825045 |
Zhengmin Liang1, Haiying Nie1, Yangfeng Xu1, Jianbo Peng2, Yun Zeng1, Yingyi Wei1, Xuemei Wen1, Jiaming Qiu3, Weiting Zhong3, Xuming Deng3, Jiakang He4.
Abstract
Rosmarinic acid (RA) is an active component of a traditional Chinese herbal medicine. Previously, we reported that RA exerted a strong anti-inflammatory effect in a mouse acute lung injury model. Therefore, we hypothesized that RA might also have potential therapeutic effects in a murine model of asthma. In this study, we aimed to evaluate the anti-asthmatic activity of RA and explored its possible molecular mechanisms of action. Female BALB/c mice that had been sensitized to and challenged with ovalbumin (Ova) were treated with RA (20mg/kg) 1h after challenge. The results showed that RA greatly diminished the number of inflammatory cells and the production of Th2 cytokines in the bronchoalveolar lavage fluid (BALF); significantly reduced the secretion of total IgE, Ova-specific IgE, and eotaxin; and markedly ameliorated airway hyperresponsiveness (AHR) compared with Ova-induced mice. Histological studies further revealed that RA substantially decreased inflammatory cells infiltration and mucus hypersecretion compared with Ova-induced mice. Moreover, our results suggested that the protective effects of RA were mediated by the inhibition of JNK and p38 MAPK phosphorylation and nuclear factor-κB (NF-κB) activation. Furthermore, RA treatment resulted in a significant reduction in the mRNA expression of AMCase, CCL11, CCR3, Ym2 and E-selectin in lung tissue. These findings suggest that RA may effectively delay the development of airway inflammation and could thus be used as a therapy for allergic asthma. Copyright ÂEntities:
Keywords: AHR; Allergic airway inflammation; MAPK; NF-κB; Rosmarinic acid; Therapeutic
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Year: 2016 PMID: 27825045 DOI: 10.1016/j.intimp.2016.10.010
Source DB: PubMed Journal: Int Immunopharmacol ISSN: 1567-5769 Impact factor: 4.932